SUMMARY A fast-neutron mutagenized population of rice seedlings was screened with Magnaporthe grisea, the causal agent of rice blast disease, to identify mutants with alterations in the defence response. Three mutant lines, ebr1, ebr2 and ebr3 (enhanced blast resistance) were identified that display enhanced resistance to M. grisea. ebr1 and ebr3 also confer enhanced resistance to the bacterial pathogen Xanthomonas oryzae pv. oryzae (Xoo). ebr3 develops a lesion mimic (LM) phenotype upon inoculation with M. grisea, and the phenotype is also induced by a shift in environmental conditions. The fourth mutant line, ncr1 (necrosis in rice), has an LM phenotype under all conditions tested and lacks enhanced resistance to either M. grisea or Xoo. Complementation testing using the mutant lines ebr3 and ncr1 indicates that the ebr3 and ncr1 loci are nonallelic and recessive. ebr1 and ebr2 display no alterations in expression of the rice pathogenesis-related (PR) genes PBZ1 and PR1, compared to wild-type CO39. ebr3 has an elevated expression of PBZ1 and PR1 only in tissue displaying the LM phenotype. ncr1 strongly expresses PBZ1 in tissue displaying the LM phenotype, whereas PR1 expression in this tissue is similar to wild-type CO39.

Several common themes have shaped the evolution of plant disease resistance genes. These include duplication events of progenitor resistance genes and further expansion to create clustered gene families. Variation can arise from both intragenic and intergenic recombination and gene conversion. Recombination has also been implicated in the generation of novel resistance specificities. Resistance gene clusters appear to evolve more rapidly than other regions of the genome. In addition, domains believed to be involved in recognitional specificity, such as the leucine-rich repeat (LRR), are subject to adaptive selection. Transposable elements have been associated with some resistance gene clusters, and may generate further variation at these complexes.